Renal function and morphology are studied in rats following exposure to toxic metal, lead or cadmium. Trace mineral excretion is measured before, during, and after therapeutic chelation. Effects of metal toxicity on renal handling of glucose are also being investigated. Parameters being measured include glucose reabsorptive capacity, glomerular filtration rate, and renal plasma flow in animals of different ages with and without toxic metal exposure. Dose-response is being studied using purified diets with defined essential metal content. Results to date indicate that lead exposure increases urinary excretion of calcium, zinc, copper, iron, and magnesium. Treatment of control and lead exposed rats with the calcium salt of EDTA produces further increased excretion of lead, zinc, copper and iron. Increased calcium excretion does not exceed the content of administered calcium chelate. Animals fed diets containing excess essential minerals and exposed to 1000 ppm lead in drinking water for periods up to 14 months (blood lead Less than 25 Mug/dl) showed no differences in maximum glucose reabsorption, glomerular filtration rate, or renal plasma flow. After seven to ten weeks of drinking water with 10,000 ppm lead (blood lead Alpha 40 Mug/dl), animals showed a small increase in glucose reabsorbtion rate; this appears to be directly related to an increase in kidney weight weight. The purpose of these studies is twofold; one is to determine the effects of specific toxic metals on renal function. The second is to determine the influence of altering dietary content of essential metals on parameters of renal toxicity and to establish dose-response relationships.